Research presented at the Psoriasis: From Gene to Clinic International Congress in London suggests that diet and lifestyle factors can contribute up to 30 per cent to the risk of psoriasis onset in people with the genetic predisposition to the condition.

Psoriasis is an inflammatory skin condition, affecting around two per cent of the population. Psoriasis occurs when a type of immune cell, called a T-cell, becomes overactive. They attack melanocytes, specialist skin cells that produce the pigment melanin, this immune response causes a growth of skin cells in the form of psoriatic plaques. However, the reason why this happens has been unclear.

Certain alleles (alternative forms of a gene) are linked with a higher risk of developing psoriasis, and HLA-C*06:02 is the main psoriasis risk gene. HLA-C*06:02 positive people are between 9- and 23-fold more likely to develop psoriasis than someone without an allele associated with the disease.

In a recent study the same authors identified that T-cells attack melanocytes in patients with psoriasis HLA-C*06:02 due to reaction against a certain a peptide (a chain of amino acids, the building blocks of proteins, amongst other things). In the skin, this peptide is only found in melanocytes, however similar peptides are also found in our external environment, including in certain foods

T-cell immune reactions are triggered by amino acid patterns. This means that peptides sharing the same amino acid pattern as the peptide in melanocytes may trigger the same psoriasis-inducing reaction. In this study the researchers used a database to find peptides which have the same amino acid pattern as seen in melanocytes. These environmental candidates were then tested for their ability to trigger the reaction that causes psoriasis.

In this way they identified a variety of peptides in proteins from human skin and gut microbiomes, the chlamydia bacterium, and from foods such as wheat, coffee, apples, and spinach, all of which brought on this reaction.

The identification of potential triggers may help to develop strategies for psoriasis prevention in individual patients, these patients and their triggers would have to be verified in clinical practice.

Dr Jörg Prinz, from the Ludwig-Maximilian-University of Munich, one of the authors of the study, said:

The aim of our study was to get a better understanding the factors at the molecular level that translate the genetic predisposition for psoriasis into the actual manifestation of the disease. Essentially, why do only some of the people who have a genetic tendency towards psoriasis have it, whilst others don’t? Our results show that lifestyle factors may be important.

These results provide initial evidence that environmental factors may serve as potential triggers for this specific autoimmune response in psoriasis. It may also have implications in understanding how environmental factors affect the risk of autoimmune diseases in general.”

Matthew Gass of the British Association of Dermatologists said:

This is very interesting research that has the potential to expand our understanding of the mechanisms that drive the development of psoriasis, but also could have practical benefits for potential patients.”

What we need now is more research that can build on these findings. In an ideal world we would have ways of identifying triggers in individual patients, to help them avoid them.

These results provide the first evidence of environmental antigens that may serve as potential triggers of the melanocyte-specific autoimmune response in psoriasis. They suggest that exposure to environmental antigens may drive priming and expansion of potentially self-reactive T cells and thus initiate autoimmune disease responses.


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